Diabetic and nondiabetic gastroparesis

Gastroparesis is a syndrome characterized by the impaired transit of food from the stomach to the duodenum in the absence of mechanical obstruction [1]. Traditionally, the term gastroparesis has been synonymous with impaired gastric motility but recently has expanded to include other abnormalities of upper gastrointestinal function, including alterations of gastric tone, myoelectric rhythms, antral contractions, pyloric relaxation, duodenal receptivity, and lack of coordination of these events .

Gastroparesis may manifest as a variety of symptoms related to the upper gastrointestinal tract, including nausea, vomiting, early satiety, postprandial bloating, distention, and abdominal pain. These symptoms are nonspecific and may suggest nonmotility sources such as peptic ulcer disease,

Gastroparesis can result from a number of disorders, but it is most commonly found in one of three clinical situations: diabetes mellitus, after gastric surgery, and when a clear source is not identifiable (idiopathic) [4•]. If a patient does not have diabetes or postsurgical status, a workup to exclude collagen vascular disorders, smooth muscle disorders, or neurologic sources is necessary before making the diagnosis of idiopathic gastroparesis [4•]. A recent study by our group [5] reviewed 146 gastroparetic patients from an academic motility referral center. Several important clinical observations were made. The most common etiology was idiopathic (35.6%), followed by diabetes (29%) and a post–gastric surgery state (13%) (Table 1, Fig. 1). The mean age of onset was 33.7 years, most of the patients were female (82%), and a

Opinion Statement • Nutritional support is essential in treating patients with gastroparesis. Initially, dietary changes should be instituted to reduce extra fat and bulk, and patients should be encouraged to eat frequent small meals with liquid supplementation. Enteral feeding should be introduced in the event of weight loss or persistent vomiting. • Medical therapy is usually necessary early in treatment. Cisapride is the initial agent of choice and may be combined with an antiemetic agent, such as promethazine or chlorpromazine or, if side effects occur, ondansetron and granesitron. If cisapride is ineffective or contraindicated, metoclopramide is a reasonable option, though limited by side effects.

Erythromycin is useful in the acute treatment of postoperative ileus and hospitalized gastroparetic patients, but its role is limited based on concerns about poor long-term effectiveness and antimicrobial resistance. Once domperidone becomes available in the United States, it will be useful for its promotility and antiemetic qualities. • Combination therapy should be considered if monotherapy with cisapride or metoclopramide alone is ineffective. While not yet well studied, combination therapy has the potential to offer dramatic benefit for patients with refractory gastroparesis. Metoclopramide may be added to cisapride for patients with breakthrough symptoms or refractory chronic symptoms.

Other combinations include metoclopramide with erythromycin, domperidone with cisapride, and domperidone with erythromycin. • In the future, gastric pacing may become an effective option for patients not responding to medical therapy. Total gastrectomy should be performed only for end-stage gastroparesis when all other therapy has failed. Both procedures should be reserved for centers that specialize in severe gastric motility disorders.mechanical obstruction, or nonulcer dyspepsia. large percentage of the women with idiopathic gastroparesis 2 Functional GI Disorders and GI Motility Dysfunction reported a history of physical or sexual abuse (62%). A history of physical abuse had a significantly higher association with abdominal pain in these patients. After 6 years of follow-up, three quarters (74%) of the patients required long-term prokinetic therapy, one fifth (21%) required nutritional support, 6% required gastric pacing, 5% required gastrectomy, and 7% died as a result of their disease, indicating a significant amount of morbidity and mortality associated with gastroparesis.

It is not always possible to correlate the symptoms of gastroparesis with abnormal testing. For example, poor concordance between the severity of symptoms and degree of motility impairment in diabetics has been reported. Delayed gastric emptying is present in up to 50% of all patients with diabetes mellitus, but frequently these abnormalities exist in the absence of symptoms (diabetics are the largest subset of gastroparetic patients studied to date) [6,7•]. Other patients may not always have objective evidence of gastroparesis but will still have significant and disabling symptoms.

The goal of treating patients with gastroparesis is twofold: to correct the underlying motility disorder and to provide symptomatic relief. Phenothiazines (promethazine and chlorpromazine) are the mainstays of traditional antiemetic therapy. Although they act at multiple central sites to control vomiting, their primary activity is through dopaminergic antagonism in the area postrema of the fourth ventricle [8]. As a result of their central mechanism of action, they are midal symptoms and sedation). Another very powerful class of centrally acting antiemetics comprises the 5HT3 antagonists. Ondansetron and granesitron are available in both oral and intravenous preparations for refractory nausea.

Established prokinetic agents include metoclopramide, cisapride, domperidone, and erythromycin. The prokinetic effect of domperidone and metoclopramide is a result of dopamine inhibition both centrally and peripherally. Metoclopramide is limited by side effects (akathisia, tremors, depression, and Parkinson-like syndrome) resulting from its affinity for the substantia nigra [8–10]. Despite its substantial side effect profile, metoclopramide still has a significant role intravenously in the treatment of acute nausea and vomiting due to its powerful antiemetic and promotility effect. It can also be very useful when given subcutaneously at home for acute exacerbations of nausea and vomiting. It has also been found to improve antroduodenal coordination [11]. Its role in chronic therapy is limited by concerns about side effects, which can result in up to 40% of patients not tolerating it.

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